Antidepressants: Benefit Of SNRI Is Proven
August 28, 2009
The Institute for Quality and Efficiency in Health Care (IQWiG) was commissioned by the Federal Joint Committee (G-BA) to investigate whether patients with depression benefit from taking drugs belonging to the selective serotonin and norepinephrine reuptake inhibitor (SNRI) drug class. Up till now, 2 of these drugs have been approved as antidepressants in Germany: venlafaxine and duloxetine. The Institute published its final report on 18 August. According to this report, the benefit of both drugs has been proven compared to a sham drug (placebo): patients respond better to the therapy and suffer less from the symptoms of depression. Moreover, there are indications that both drugs protect against relapse in addition to alleviating symptoms.
The Path to New Antibiotics
August 27, 2009
Researchers at Burnham Institute for Medical Research (Burnham), University of Texas Southwestern Medical Center and University of Maryland have demonstrated that an enzyme that is essential to many bacteria can be targeted to kill dangerous pathogens. In addition, investigators discovered chemical compounds that can inhibit this enzyme and suppress the growth of pathogenic bacteria. These findings are essential to develop new broad-spectrum antibacterial agents to overcome multidrug resistance. The research was published in the Cell journal Chemistry & Biology on August 27.
Andrei Osterman, Ph.D., an associate professor in Burnham’s Bioinformatics and Systems Biology program, and colleagues, targeted the bacterial nicotinate mononucleotide adenylyltransferase (NadD), an essential enzyme for nicotinamide adenine dinculeotide (NAD) biosynthesis. NAD has many crucial functions in nearly all important pathogens and the bacterial NadD differs significantly from the human enzyme.
“It’s clear that because of bacterial resistance, we need new, wide-spectrum antibiotics,” said Dr. Osterman. “This enzyme is indispensable in many pathogens, so finding ways to inhibit it could give us new options against infection.”
Beta-blockers and Stroke – New Insights Into Their Use For Older People
August 27, 2009
A University of Leicester-led study may have uncovered the reason why Beta-blockers are less effective at preventing stroke in older people with high blood pressure, when compared to other drugs for high blood pressure.
The research, carried out by Bryan Williams, Professor of Medicine at the University of Leicester, and his colleague Dr. Peter Lacy, has been published in the prestigious Journal of the American College of Cardiology and has been cited on the MDLinx.com site as currently the world’s number one leading finding in its field.
Professor Williams’ research shows that lowering heart rate in older people, as Beta blockers do, can have a potentially detrimental effect on central aortic pressures (pressures in the large arteries close to the heart).
He commented: “Such findings can help define the template for optimal treatment strategies and highlight why new methods to estimate central aortic pressures are providing new insights into the pathogenesis of cardiovascular disease and how new drugs can be tailored to limit the damage.
Research Shows Why Low Vitamin D Raises Heart Disease Risks In Diabetics
August 26, 2009
Low levels of vitamin D are known to nearly double the risk of cardiovascular disease in patients with diabetes, and researchers at Washington University School of Medicine in St. Louis now think they know why.
A healthy macrophage cell, at left, with sufficient vitamin D. On the right, a macrophage with inadequate vitamin D has become clogged with cholesterol, an early marker of atherosclerosis.
They have found that diabetics deficient in vitamin D can’t process cholesterol normally, so it builds up in their blood vessels, increasing the risk of heart attack and stroke. The new research has identified a mechanism linking low vitamin D levels to heart disease risk and may lead to ways to fix the problem, simply by increasing levels of vitamin D.
“Vitamin D inhibits the uptake of cholesterol by cells called macrophages,” says principal investigator Carlos Bernal-Mizrachi, M.D., a Washington University endocrinologist at Barnes-Jewish Hospital. “When people are deficient in vitamin D, the macrophage cells eat more cholesterol, and they can’t get rid of it. The macrophages get clogged with cholesterol and become what scientists call foam cells, which are one of the earliest markers of atherosclerosis.”
Long-Term Tamoxifen Use Increases The Risk Of An Aggressive, Difficult To Treat Type Of Second Breast Cancer
August 25, 2009
While long-term tamoxifen use among breast cancer survivors decreases their risk of developing the most common, less aggressive type of second breast cancer, such use is associated with a more than four-fold increased risk of a more aggressive, difficult-to-treat type of cancer in the breast opposite, or contralateral, to the initial tumor. These findings by Christopher Li, M.D., Ph.D., and colleagues at Fred Hutchinson Cancer Research Center were published online Aug. 25 in the journal Cancer Research.
Hormonal therapy with drugs like tamoxifen is one of the most common treatments for breast cancer because it has been shown to reduce the risk of dying from the disease but, as this study suggests, it does have risks.
Comparing breast-cancer patients who received the estrogen-blocking drug tamoxifen to those who did not, the researchers found that while the drug was associated with a 60 percent reduction in estrogen receptor-positive, or ER positive, second breast cancer – the more common type, which is responsive to estrogen-blocking therapy – it also appeared to increase the risk of ER negative second cancer by 440 percent. “This is of concern, given the poorer prognosis of ER-negative tumors, which are also more difficult to treat,” said Li, an associate member of the Hutchinson Center’s Public Health Sciences Division.
Understanding Intrinsic Changes in Protein Shape Could Lead to New Drugs
August 24, 2009
Computational biologists at the University of Pittsburgh School of Medicine have shown that proteins have an intrinsic ability to change shape, and this is required for their biological activity. This shape-changing also allows the small molecules that are attracted to a given protein to select the structure that permits the best binding. That premise could help in drug discovery and in designing compounds that will have the most impact on protein function to better treat a host of diseases.
The findings were published this week in the online version of the Proceedings of the National Academy of Sciences.
According to the classical view, known as “induced fit,” drug binding causes a change in the target protein structure, explained senior author Ivet Bahar, Ph.D., professor and John K. Vries Chair of the Department of Computational Biology, Pitt School of Medicine. But it now appears that a protein has many different conformations that are already available even without the presence of a binding molecule, which is called the ligand. The ligand attaches to the protein shape that allows it to fit well, and that close interaction can lead to effective inhibition of protein function.
Yale Researcher Questions Federal Guidelines for Seasonal and Swine Flu Vaccines
August 24, 2009
With the seasonal flu season approaching and uncertainty over whether swine flu will become more severe, new research published by Yale School of Public Health has found that more people are likely to avoid illness if vaccines are given out first to those most likely to transmit viruses, rather than to those at highest risk for complications. This research differs from current vaccination recommendations of the Centers for Disease Control (CDC) and the Advisory Committee on Immunization Practices (ACIP).
The Yale study appears in the August 20 issue of the journal Science online at the Science Express website, http://www.sciencemag.org/sciencexpress .
It will be published in the print journal Science at a later date.
Vitamin-A Derivative Provides Clues To Better Breast Cancer Drugs
August 23, 2009
Retinoic acid, a derivative of vitamin A, could lead researchers to a new set of drug targets for treating breast cancer, researchers from the University of Chicago report in the June 26, 2009, issue of the journal Cell.
The most common forms of breast cancer are fueled by the female hormone estrogen. By comparing the effects of estrogen and retinoic acid on the entire genome, the researchers found that they have a “yin-yang” effect. They alter the expression of many of the same genes, with estrogen tipping the scales towards cell proliferation and retinoic acid restoring the balance by inhibiting cellular growth.
This balanced control of gene expression regulates fundamental cellular processes, say the authors. When it is dysregulated, it can lead to cancer.
New Discovery Points The Way Towards Malaria Vaccine
August 23, 2009
Malaria kills anywhere from one to three million people around the world annually and affects the lives of up to 500 million more. Yet until now, scientists did not fully understand exactly how the process that caused the disease’s severe hallmark fevers began.
A team led by Dr. Martin Olivier from the Research Institute of the McGill University Health Centre (RI-MUHC) and McGill University in Montreal has solved this mystery, and may have blazed a trail towards the development of vaccine-like treatments to limit the severity of the devastating parasitic ailment. . The results of their study will be published August 21 in the journal PLoS Pathogens.
Malaria is a mosquito-borne infectious disease spread by parasites from the Plasmodium family. Inside the human body, the malaria parasite infects red blood cells where it survives and reproduces by feeding on the cells’ contents. Eventually the cells burst, releasing the parasites and also a waste byproduct of their reproductive process: hemozoin.
Princeton Team Learns Why Some Antibiotics Pack Such A Punch
August 22, 2009
By studying the intricate mechanisms at work in protein production, a Princeton-led team has discovered why certain kinds of antibiotics are so effective. In doing so, they also have discovered how one protein protects against cell death, shedding light on a natural cancer-fighting process.
In a study appearing in the Aug. 7 edition of the journal Science, Thomas Silhavy, Princeton’s Warner-Lambert Parke-Davis Professor of Molecular Biology, and Johna van Stelten, a graduate student, working with two Swiss researchers have uncovered how some antibiotics in common use for 50 years — tetracycline and chloramphenicol — can be so lethal against certain strains of bacteria.
Simply put, these drugs plug things up.